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1BP-LSD
1BP-LSD (1-boronobenzoyl-lysergic acid diethylamide) is a synthetic psychedelic of the lysergamide class. It is a direct prodrug of LSD — the first lysergamide to incorporate a boron atom.[1] It activates serotonin receptors in the brain, producing the visual and cognitive shifts characteristic of classical psychedelics.[2]
1BP-LSD (1-boronobenzoyl-lysergic acid diethylamide) is an emerging synthetic psychedelic of the lysergamide class. It is the latest N1-acyl prodrug of LSD and the first lysergamide to incorporate a boron atom.[1] 1BP-LSD is presumed to act as a 5-HT₂A receptor agonist through its active metabolite LSD, which disrupts the brain's default filtering of sensory and cognitive input.[2]
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1BP-LSD appeared on research chemical markets in December 2025, weeks after Germany banned its predecessor 1S-LSD.[3] It is the latest in a decade-long succession of N1-acyl LSD analogs, each engineered with a novel chemical group to stay outside German drug law. As of May 2026, it circulates on international research chemical markets — legal in Germany but legally ambiguous in most other countries.
Subjective effects include geometric visual patterns, brightened colors, thought connectivity, emotional intensification, and ego dissolution. The experience mirrors LSD — expansive, stimulant-edged, and mentally sharp — but arrives through a slow come-up that can stretch two or more hours.[4] Thought loops, anxiety during the long come-up, and difficulty sleeping are common unwanted effects.
1BP-LSD produces no physical dependence, and no death has been attributed to its active metabolite LSD.[5] The primary danger is psychological — high doses in unsupported settings can trigger acute panic, and people with a personal or family history of psychosis face disproportionate risk of lasting destabilization.[6] No peer-reviewed data exist for 1BP-LSD itself; all characterization comes from LSD and the broader N1-acyl prodrug series.[7][8]
History[edit]
Emergence
1BP-LSD appeared on research chemical markets in December 2025, weeks after Germany banned its predecessor 1S-LSD.[3] Its boron-containing N1 substituent was designed to fall outside every structural group defined in German scheduling law.[9] No peer-reviewed study of the compound had been published as of May 2026 — consistent with earlier N1-acyl analogs taking one to two years to receive forensic characterization.[10]
The N1-acyl succession
1BP-LSD is the latest in a decade-long series of N1-acyl LSD analogs, each designed to exploit structural gaps in Germany's drug scheduling law. The sequence runs from ALD-52 through 1P-LSD,[10] 1B-LSD,[11] 1cP-LSD,[12] 1V-LSD,[13] and 1S-LSD[14] — each eventually banned by ministerial amendment. 1BP-LSD's unprecedented boron atom represents the series' latest structural leap.
Regulatory catalyst
Germany banned 1S-LSD effective November 21, 2025.[3] An earlier attempt to ban all LSD analogs as a single structural group failed on constitutional grounds, forcing compound-by-compound scheduling.[15] 1BP-LSD's boron atom was a structural departure large enough to evade the updated definitions.
The name "1BP-LSD" follows the established naming convention for N1-acyl LSD analogs: the prefix denotes the N1 substituent, here "BP" for boronopinacolbenzoyl. The compound is sold on blotter paper at 175–200 µg per tab,[4] maintaining the distribution format that has defined LSD since the 1960s. Its emergence alongside 1FE-LSD illustrates how quickly the research chemical market generates structural solutions to scheduling pressure.
Chemistry[edit]
Structural class
1BP-LSD belongs to the lysergamide family, built on the same tetracyclic ergoline scaffold as LSD. It is LSD with a large N1-acyl group added at the indole nitrogen — a modification that renders it inactive until the body strips the group and releases LSD. The molecular formula is C₃₇H₄₈BN₃O₄ (609.37 g/mol).[1]
The N1 substituent includes an aromatic ring bonded to the indole nitrogen, with a cyclic boronate ester group at its end — making 1BP-LSD the first lysergamide to incorporate a boron atom.[1]
A discrepancy exists between the popular name and the vendor-reported molecular formula. The popular name implies a molecular weight near 505 g/mol; the vendor formula (C₃₇H₄₈BN₃O₄, 609.37 g/mol) supports a different structure.[1] One consumer source reports "pinacol" as a hydrolysis product, implying yet another structure.[4] This discrepancy requires independent forensic confirmation. All data in this article uses the vendor formula pending peer-reviewed confirmation.
Pharmacology[edit]
Prodrug mechanism
1BP-LSD is a prodrug — the intact compound has little direct activity and must convert to LSD in the body before producing effects.[7][8] Conversion happens in two steps[4]: the boronate ester breaks apart first, then a second enzyme strips the remaining N1 group and releases LSD. This two-step process is estimated to take about 2 hours — far longer than simpler prodrugs like 1P-LSD.
Primary target
Once LSD is released, it activates serotonin receptors in the prefrontal cortex.[2] A structural flap in the receptor closes over LSD and traps it there, producing unusually long receptor engagement.[16] LSD also engages dopamine and adrenergic receptors,[17] which accounts for its stimulant quality and mild vascular effects.[18]
Pharmacokinetics
No human pharmacokinetic data exist for 1BP-LSD. For LSD itself, oral bioavailability is about 80%,[19] with blood levels peaking about 1.1 hours after direct dosing.[20] For 1BP-LSD, peak effects are estimated at 3–4 hours total due to the added conversion step. People who process drugs slowly through a particular liver enzyme experience about 75% greater drug exposure and stronger effects.[21]
Neuroscience[edit]
All neuroscience findings derive from studies of LSD. As a prodrug that releases LSD as its sole active metabolite, 1BP-LSD is expected to produce identical neural effects once conversion is complete.
Where it acts
LSD activates serotonin receptors on neurons in the prefrontal cortex, disrupting the brain's normal filtering of sensory input and flooding perception with unfiltered data.[22] The brain network associated with the sense of self loses internal coherence — the neural correlate of ego dissolution. Brain regions that don't normally communicate begin exchanging signals, producing the sense of unity and interconnectedness and novel conceptual connections.[22]
Why it matters
The REBUS model proposes that LSD weakens the brain's top-down predictive models, allowing raw sensory experience to drive perception more directly.[22] This makes the brain more responsive to whatever surrounds the experience — which is why the psychological and physical setting shape the outcome so strongly. LSD also promotes growth of new brain connections through signaling involving growth factors.citation needed
Key uncertainties for 1BP-LSD include whether its slower, two-step LSD release alters the temporal dynamics of neural effects. A gradual rise in receptor occupancy could engage brain networks differently than direct LSD administration. Individual variation in boronate ester hydrolysis may also produce meaningfully different onset profiles between users.
Subjective Effects[edit]
The 1BP-LSD experience is, in all observable respects, the LSD experience delivered slowly. The two-step prodrug conversion produces a gradual come-up stretching two or more hours, building toward the same expanded, stimulant-edged, visually vivid state as direct LSD.[4]
Compared to psilocybin, 1BP-LSD carries a sharper cognitive quality, more stimulant energy, and a longer total duration.[18] Relative to direct LSD, the difference is purely kinetic — a slower ramp into the same experiential space.[7]
1BP-LSD appeared on research chemical markets in December 2025, weeks after Germany banned its predecessor 1S-LSD under the Neue-psychoaktive-Stoffe-Gesetz.[3] It continues a decade-long succession of N1-acyl LSD prodrugs — each engineered to evade German scheduling and each eventually captured by regulatory amendment. As of May 2026, it circulates on international research chemical markets, legal in Germany but ambiguous in most other jurisdictions.
Subjective effects include geometric visual patterns, thought connectivity, ego dissolution, and emotional intensification. The experience mirrors LSD in character — expansive, stimulant-edged, and cognitively sharp — but arrives through a notably slower onset due to two-step prodrug hydrolysis.[4] Thought loops, anxiety during the extended come-up, and difficulty sleeping are common unsought effects.
1BP-LSD produces no physical dependence, and no deaths have been attributed to its active metabolite LSD[5] — rapid tolerance after a single dose makes compulsive use self-limiting.[6] The primary risk is psychological: high doses in unsupported settings can trigger acute panic, and individuals with psychotic-spectrum vulnerability face disproportionate risk of lasting destabilization.[7] No peer-reviewed data exist for 1BP-LSD itself; all characterization rests on LSD and the N1-acyl prodrug series.[8][9]
History[edit]
Emergence
1BP-LSD appeared on research chemical markets in December 2025, weeks after Germany banned its predecessor 1S-LSD.[3] Its novel boron-containing N1 substituent was engineered to fall outside every structural group defined in German scheduling law.[10] No peer-reviewed analytical, pharmacological, or clinical study has been published on the compound as of May 2026 — consistent with its recent emergence, as earlier N1-acyl analogs took one to two years to receive forensic characterization.[11]
The N1-acyl succession
1BP-LSD is the latest entry in a decade-long series of N1-acyl LSD prodrugs, each designed to exploit structural gaps in Germany's Neue-psychoaktive-Stoffe-Gesetz (NpSG). The sequence began with ALD-52 and continued through 1P-LSD,[11] 1B-LSD,[12] 1cP-LSD,[13] 1V-LSD,[14] and 1S-LSD[15] — each bearing a progressively more elaborate substituent at the indole nitrogen, and each eventually captured by ministerial ordinance.
Regulatory catalyst
The direct trigger for 1BP-LSD's creation was the Sixth Ordinance amending the NpSG annex, which banned 1S-LSD effective November 21, 2025.[3] An earlier proposal to ban all LSD analogs as a single structural group had been rejected on constitutional grounds; regulators instead pursued compound-by-compound scheduling.[16] 1BP-LSD's boron atom — unprecedented in the lysergamide class — represented a structural departure large enough to evade the amended definitions.
The name "1BP-LSD" follows the established naming convention for N1-acyl LSD analogs: the prefix denotes the N1 substituent, here "BP" for boronopinacolbenzoyl. The compound is sold on blotter paper at 175–200 µg per tab,[4] maintaining the distribution format that has defined LSD since the 1960s. Its emergence alongside 1FE-LSD — another novel successor — illustrates the speed at which the research chemical market iterates on structural solutions to scheduling pressure.
Chemistry[edit]
Structural class
1BP-LSD belongs to the lysergamide family, built on the tetracyclic ergoline scaffold shared with LSD. It retains LSD's complete molecular architecture — the diethylamide at C-9 and the N-methyl at N-6 — with a large N1-acyl substituent that distinguishes it from all prior analogs in the series.
Where earlier N1-acyl LSD prodrugs (ALD-52, 1P-LSD, 1B-LSD, 1cP-LSD, 1V-LSD, 1S-LSD) employed simple aliphatic chains at N1, 1BP-LSD introduces an aromatic benzoyl linker bearing a cyclic boronate ester — making it the first lysergamide to incorporate a boron atom.[1]
Molecular properties
| Molecular formula | C₃₇H₄₈BN₃O₄ |
| Molecular weight | 609.37 g/mol |
The N1 substituent consists of a benzoyl carbonyl attached to the indole nitrogen, with the para position of the benzene ring bearing a 1,3,2-dioxaborolane heterocycle flanked by four ethyl groups (tetraethyl boronate ester).[1] This adds approximately 286 g/mol to LSD's base molecular weight of 323.4 g/mol — nearly doubling the parent compound's mass.
Stereochemistry
1BP-LSD retains the (6aR,9R) absolute configuration of the ergoline scaffold, consistent with d-lysergic acid diethylamide.[1] The N1-acyl substituent does not introduce additional stereocenters. Only the (6aR,9R) diastereomer is expected to carry significant activity at serotonin receptors.
Chemical identity discrepancy
A significant discrepancy exists between the commonly cited popular name and the vendor-reported molecular formula. The popular name describes a propionyl chain with a tetramethyl (pinacol-type) boronate ester, which would yield a molecular weight near 505 g/mol. The vendor formula (C₃₇H₄₈BN₃O₄, 609.37 g/mol) instead supports a benzoyl linker with a tetraethyl boronate ester.[1] One consumer source reports "pinacol" as a hydrolysis product, which would imply the tetramethyl structure.[4] This discrepancy requires resolution by independent forensic characterization. All data in this article uses the vendor formula pending peer-reviewed confirmation.
Pharmacology[edit]
Prodrug mechanism
1BP-LSD functions as a prodrug for LSD. Like other N1-acyl lysergamides, the intact compound has little or no direct activity at serotonin receptors and must be converted to LSD in the body to produce psychedelic effects.[8] The strongest human evidence for this prodrug class comes from a study of oral 1P-LSD, where only LSD — not the intact prodrug — was detectable in blood and urine.[9]
For 1BP-LSD, conversion is proposed to occur in two steps.[4] First, the cyclic boronate ester cleaves under physiological conditions, producing a 4-hydroxybenzoyl-LSD intermediate. Second, enzymes cleave the amide bond at N1, releasing LSD and 4-hydroxybenzoic acid as co-products.
This two-step process is expected to delay onset significantly — an estimated 2 hours for complete conversion, compared to 30–60 minutes for simpler prodrugs like 1P-LSD.[4] No controlled pharmacokinetic data for 1BP-LSD exist to confirm this estimate.
Primary target
Once liberated, LSD acts principally through 5-HT₂A receptor agonism — confirmed by complete blockade of all subjective effects with the selective antagonist ketanserin.[2] LSD's unusually long receptor engagement arises from a structural feature: an extracellular loop folds over the binding pocket and traps the molecule, producing slow dissociation.[17]
Beyond 5-HT₂A, LSD engages a broad range of serotonin, dopamine, and adrenergic receptors.[18] This multi-receptor profile — including partial activity at dopamine D₁/D₂ and 5-HT₁A — contributes to the compound's stimulant quality, mood modulation, and ergot-like vasoconstriction.[19]
Pharmacokinetics
No human pharmacokinetic data exist for 1BP-LSD. For LSD itself, oral bioavailability is approximately 80%,[20] and time to peak plasma concentration is about 1.1 hours after direct administration.[21] For 1BP-LSD, peak effects are expected substantially later — an estimated 3–4 hours total — due to the additional prodrug conversion step.
LSD's half-life ranges from 2.7–3.5 hours at low doses to 6.4 hours at full psychedelic doses.[21][9] Less than 1% is metabolized within 4 hours in liver tissue, which helps explain the compound's prolonged duration.[22] Individuals who metabolize drugs slowly through the CYP2D6 pathway experience approximately 75% greater overall drug exposure and stronger subjective effects.[23]
Neuroscience[edit]
All neuroscience findings derive from studies of LSD; no brain imaging or electrophysiology studies have been conducted with 1BP-LSD. As a prodrug that liberates LSD as its sole active metabolite, 1BP-LSD is expected to produce identical neural effects once conversion is complete.
Where it acts
LSD activates 5-HT₂A receptors on pyramidal neurons in the prefrontal cortex, triggering cascading effects across brain networks.[24] The default mode network — associated with self-referential thought and narrative identity — loses internal coherence, an effect that correlates with subjective ego dissolution.
Simultaneously, thalamic gating of sensory input weakens, flooding the cortex with unfiltered perception and driving the synesthesia and perceptual intensification characteristic of the psychedelic state.[24] Brain regions that do not normally communicate begin exchanging information, producing the sense of unity and interconnectedness and novel conceptual linkages reported by users.[24]
Why it matters
The REBUS model (Relaxed Beliefs Under Psychedelics) proposes that LSD weakens the brain's top-down predictive models, allowing raw sensory data to drive experience more freely.[24] This framework explains both the perceptual novelty and the heightened sensitivity to environment — weakened priors make the brain more responsive to whatever context surrounds the experience.
LSD also promotes structural neuroplasticity — dendritic growth and new synaptic connections — through BDNF and mTOR signaling pathways.citation needed This neuroplastogenic activity may contribute to lasting psychological shifts reported after psychedelic experiences.
Key uncertainties for 1BP-LSD include whether its slower, two-step LSD release alters the temporal dynamics of neural effects — a gradual rise in receptor occupancy could engage brain networks differently than the rapid onset of direct LSD administration. Individual variation in boronate ester hydrolysis efficiency may also produce meaningfully different neural response profiles between users, though whether this translates to qualitative experiential differences or merely variable onset times remains unknown.
Subjective Effects[edit]
The 1BP-LSD experience is, by all available evidence, the LSD experience delivered through a slower pharmacokinetic envelope. The two-step prodrug hydrolysis produces a gradual come-up — substantially longer than LSD or simpler prodrugs like 1P-LSD[4] — that may be misinterpreted as insufficient dosing, creating premature redosing risk. Set and setting remain the dominant non-pharmacological determinants of experience quality.[24]
Compared to psilocybin, which shares 5-HT₂A-mediated psychedelia but lacks LSD's dopaminergic and adrenergic engagement, 1BP-LSD (via its LSD metabolite) carries the characteristic lysergamide stimulant quality, sharper cognitive clarity, and longer total duration.[19] Relative to direct LSD, the distinction is kinetic rather than pharmacodynamic — a slower ramp into and potentially out of the experience, with the same receptor target and phenomenological space once conversion is complete.[8]
Effect Grid
At common doses (150–200 µg 1BP-LSD, delivering approximately 80–106 µg LSD-equivalent), the full psychedelic experience unfolds. Geometry becomes clearly visible — patterning on surfaces, symmetrical texture repetition, and visual drifting. Color enhancement and color alteration are prominent. Thought connectivity deepens, linking concepts across domains. Emotional enhancement intensifies both positive and challenging feelings. Music enhancement is often reported as a highlight of this dose range.
Stimulation is noticeable — wakefulness and restlessness accompany the cognitive and perceptual shifts. Pupil dilation is marked. Appetite suppression is typical, and mild nausea may occur during the come-up. Vasoconstriction and muscle tension are possible but usually mild. Sleep is effectively impossible for 10+ hours after ingestion.
This is the dose range targeted by vendor blotter tabs (175–200 µg). The ego remains intact but perspective is shifted. Introspection enhancement and novelty enhancement make familiar environments feel fresh. Time alteration — usually experienced as dilation — is common.
Modeled from the effect's dose-dependence curve — not per-substance measurements.
Visual breathing · Visual drifting · After-images · Auditory enhancement · Brightness alteration · Tracers · Visual morphing · Holotropic state · Auditory distortion · Depth perception distortion · Environmental patterning · Light sensitivity · Peripheral vision distortion · Perspective distortion · Sound sensitivity · Symmetrical texture repetition · Touch enhancement · Auditory misinterpretation · Ganzfeld effect · Peripheral misidentification · Proprioceptive distortion · Sleep-transition hallucinations · Spatial disorientation · Synesthesia · Vestibular distortion · Visual diffraction · Visual haze / noise · Visual melting · Visual acuity enhancement · Visual processing acceleration · Dreaming enhancement · Visual magnification · Olfactory enhancement · Taste enhancement · Flashbacks · Tinnitus · Internal hallucinations · Object transformations · External hallucinations · Object activation · Perspective hallucinations · Visual recursion · Auditory hallucinations · Environmental orbism / cubism · Visual flipping · Visual scenery slicing
Brightness alteration · Tracers · Visual morphing · Holotropic state · Auditory distortion · Depth perception distortion · Environmental patterning · Light sensitivity · Peripheral vision distortion · Perspective distortion · Sound sensitivity · Symmetrical texture repetition · Touch enhancement · Auditory misinterpretation · Ganzfeld effect · Peripheral misidentification · Proprioceptive distortion · Sleep-transition hallucinations · Spatial disorientation · Synesthesia · Vestibular distortion · Visual diffraction · Visual haze / noise · Visual melting · Visual acuity enhancement · Visual processing acceleration · Dreaming enhancement · Visual magnification · Olfactory enhancement · Taste enhancement · Flashbacks · Tinnitus · Internal hallucinations · Object transformations · External hallucinations · Object activation · Perspective hallucinations · Visual recursion · Auditory hallucinations · Environmental orbism / cubism · Visual flipping · Visual scenery slicing
Stimulation · Wakefulness · Body high · Appetite suppression · Heart rate perception changes · Laughter fits · Muscle tension · Physical fatigue · Restlessness · Spontaneous body sensations · Tactile euphoria · Tingling / electric sensations · Bodily lightness · Body schema distortion · Dizziness · Dry mouth · Excessive sweating · Headache · Nausea · Sexual arousal enhancement · Vibrations / buzzing · Bodily pressures · Breathing alteration · Bruxism · Dehydration sensation · Involuntary body movements · Nystagmus (eye wobbles) · Pain suppression · Respiratory stimulation · Trembling · Vasoconstriction · Abnormal heartbeat · Sexual arousal suppression · Watery eyes · Vomiting · Bodily dissociation · Tactile hallucination
Appetite suppression · Heart rate perception changes · Laughter fits · Muscle tension · Physical fatigue · Restlessness · Spontaneous body sensations · Tactile euphoria · Tingling / electric sensations · Bodily lightness · Body schema distortion · Dizziness · Dry mouth · Excessive sweating · Headache · Nausea · Sexual arousal enhancement · Vibrations / buzzing · Bodily pressures · Breathing alteration · Bruxism · Dehydration sensation · Involuntary body movements · Nystagmus (eye wobbles) · Pain suppression · Respiratory stimulation · Trembling · Abnormal heartbeat · Sexual arousal suppression · Watery eyes · Vomiting · Bodily dissociation · Tactile hallucination
Cognitive euphoria · Cognitive flexibility · Conceptual thinking · Immersion enhancement · Increased nature relatedness · Multiple thought streams · Novelty enhancement · Pattern recognition enhancement · Thought connectivity · Thought acceleration · Thought loops · Creativity enhancement · Humor enhancement · Analysis enhancement · Cognitive fatigue · Cognitive impairment · Confusion · Memory fragmentation · Memory replays · Synchronicity · Thought disorganization · Focus enhancement · Information processing enhancement · Language enhancement · Motivation enhancement · Analysis suppression · Cognitive dysphoria · Focus suppression · Information processing suppression · Memory suppression · Motivation suppression · Thought organization · Delusions of sobriety · Language suppression · Amnesia · Delusions · Delirium
Immersion enhancement · Increased nature relatedness · Multiple thought streams · Novelty enhancement · Pattern recognition enhancement · Thought connectivity · Thought acceleration · Thought loops · Creativity enhancement · Humor enhancement · Analysis enhancement · Cognitive fatigue · Cognitive impairment · Confusion · Memory fragmentation · Memory replays · Synchronicity · Thought disorganization · Focus enhancement · Information processing enhancement · Language enhancement · Motivation enhancement · Analysis suppression · Cognitive dysphoria · Focus suppression · Information processing suppression · Memory suppression · Motivation suppression · Thought organization · Language suppression · Amnesia · Delusions · Delirium
Simultaneous emotions · Anxiety · Catharsis · Empathy enhancement · Anxiety suppression · Dysphoria · Irritability
Anxiety suppression · Dysphoria · Irritability
Emotional susceptibility · Trust enhancement · Communication enhancement · Depersonalization · Sociability enhancement · Flow state · Automaticity · Compulsive behavior reduction · Ego inflation · Communication suppression · Sociability suppression · Social disconnection · Boundary dissolution · Cognitive disconnection · Ego dissolution · Identity alteration · Telepathic feelings
Sociability enhancement · Flow state · Automaticity · Compulsive behavior reduction · Ego inflation · Communication suppression · Sociability suppression · Social disconnection · Boundary dissolution · Cognitive disconnection · Ego dissolution · Identity alteration · Telepathic feelings
Time cessation
Non-dual awareness · Transpersonal memory access · Transpersonal visions · Death-rebirth sequence · Voidness · Cessation · Near-death experience
Voidness · Cessation · Near-death experience
Lucidity enhancement · Anticipatory response · Recursive awareness
Timeline
Slow emergence of first alerts as boronate ester hydrolysis begins. Subtle body awareness, mild mood shift, possible slight perceptual sharpening. Most users will not identify clear effects during this phase.
Progressive build of perceptual and cognitive effects as LSD is liberated from the prodrug. Nausea possible. Anticipatory anxiety may arise.
Full expression of psychedelic effects — geometry, color enhancement, visual drifting, thought connectivity, emotional intensification. Ego dissolution possible at strong doses. Music enhancement and time alteration are prominent.
Gradual reduction of visual and cognitive effects. Stimulation and wakefulness persist. Introspective quality deepens as perceptual intensity recedes.
Residual mood elevation, mild perceptual sensitivity, and possible creative or reflective mindset. Insomnia may persist for several hours. Some users report subtle visual phenomena for 24+ hours.
Safety[edit]
- Acute toxicity
- Low
- Chronic toxicity
- Low
- Withdrawal
- None
- Tolerance buildup
- rapid
- Tolerance reset
- 10 days
- Physical
- None
- Psychological
- Negligible
- Compulsive redosing
- Negligible
- Dose escalation
- Negligible
- Cross-tol.
- LSD · psilo · DMT
No peer-reviewed toxicological, pharmacological, or clinical safety data have been published for 1BP-LSD. All safety information below is inferred from the well-characterized parent compound LSD and the N1-acyl lysergamide prodrug class. The absence of substance-specific data reflects the compound's December 2025 emergence, not a confirmed absence of risk.
Toxicity
Acute toxicity
LSD has no established lethal dose in humans — no confirmed death has been attributed to its direct pharmacological effects despite seven decades of widespread use.[5] Computational toxicity modeling of related N1-acyl LSD analogs predicted lethal doses in rats thousands of times higher than a typical human dose.[23] 1BP-LSD was not included in these models. safety citation needed
Breakdown product toxicity
The byproducts of 1BP-LSD hydrolysis — including 4-hydroxybenzoic acid, a diol, and trace boron — are released in quantities far below any known acute toxicity threshold.[4] Long-term effects of repeated boron exposure from chronic use have not been studied.
Psychological risks
Anxiety and panic are the most common acute adverse effects, occurring more frequently at higher doses and in unsupported settings.[22] High doses can also produce paranoia, hallucinations, and disordered thinking, particularly in those with a personal or family history of psychotic disorders.[6] Rarely, visual disturbances — geometry, after-images, tracers, visual noise — persist weeks to months after last use.[24][25]
A large survey found 8.9% of psychedelic users reported functional impairment lasting more than one day, and 2.6% sought medical or psychiatric help.[26] Risperidone specifically worsens the persistent visual disturbance condition and is contraindicated.[25] LSD-class psychedelics can also trigger latent psychiatric conditions in genetically vulnerable individuals.[6]
Tolerance and dependence
Rapid tolerance develops via serotonin downregulation after a single dose, requiring 7–14 days for full recovery.[27] Cross-tolerance exists with other serotonergic psychedelics, including psilocybin and mescaline.[11][27] This rapid tachyphylaxis acts as a built-in brake against frequent use.
No physical dependence or withdrawal has been observed. The rapid tolerance and weak dopamine reinforcement make classical psychedelics among the least dependence-forming substance classes.
Drug Interactions
All interaction data is inferred from LSD; no 1BP-LSD-specific interaction studies exist. The extended onset creates a specific risk: users may take other substances during the delay, not realizing 1BP-LSD is still absorbing. Lithium combined with psychedelics is associated with seizure risk and severely difficult experiences;[26] MAOIs amplify and prolong effects through serotonin accumulation — unpredictably and dangerously; Tramadol carries a risk of dangerous serotonin overload.
MDMA raises LSD blood levels, prolongs effects, and increases cardiovascular strain by slowing LSD metabolism.[28] Chronic SSRI/SNRI use reduces psychedelic effects but does not eliminate serotonin syndrome risk. Antipsychotics block psychedelic effects; risperidone also worsens the persistent visual disturbance condition.[25] Cannabis intensifies and extends effects unpredictably.
Contraindications
8 knownAll contraindications are inferred from LSD and the serotonergic psychedelic class.
Absolute contraindications:
- Personal or family history of psychosis or schizophrenia: LSD-class psychedelics can trigger acute psychotic episodes and may precipitate chronic psychotic illness in predisposed individuals.[6]
- Current lithium use: Associated with significantly increased seizure risk and severe adverse reactions.[26]
- Current MAOI use: Risk of severe, unpredictable serotonergic potentiation.
Relative contraindications:
- Bipolar disorder with psychotic features: Risk of manic or psychotic episode.
- Current mood stabilizer use: Associated with increased risk of challenging experiences.[26]
- Heart conditions: LSD produces moderate increases in heart rate and blood pressure.[22]
- Pregnancy and breastfeeding: No safety data exist. safety citation needed
- Seizure disorders: The interaction between psychedelic brain excitation and lowered seizure thresholds is unstudied. safety citation needed
Harm Reduction[edit]
Forms & Identification
1BP-LSD circulates exclusively as blotter paper. Blotters are visually identical regardless of their active compound, so confirming identity requires reagent testing. Standard reagent kits may not reliably distinguish 1BP-LSD from other lysergamides — no published reagent reaction profiles exist for this compound.
The extended onset (2–3 hours) is the most consequential practical risk. Users accustomed to 30–60 minute onsets from LSD or 1P-LSD may interpret the delay as inactive material and redose prematurely. The result can be a doubled dose arriving as a single wave.
Guidelines
- Test the material using available reagent kits, accepting that results may not distinguish between lysergamides.
- Start with a lower dose — individual variation in onset timing and intensity may be greater than with simpler prodrugs.
- Wait at least 3 hours before considering whether effects have fully materialized. Premature redosing is the most common practical risk with slow-onset prodrugs.
- Prepare the environment in advance: comfortable temperature, accessible water, minimal obligations for 14+ hours, no driving requirement.
- Eat a light meal 2–3 hours before dosing. An empty stomach may speed onset; a heavy meal may extend the already long delay unpredictably.
- Tell someone the plan, substance, and dose — even when using alone.
Set & Setting
As with all serotonergic psychedelics, the psychological context (set) and physical environment (setting) are the primary determinants of experience quality.[22] The extended come-up places particular demands on both — two hours of uncertainty about whether effects will arrive can generate anticipatory anxiety that colors the entire experience.
A calm, familiar environment with trusted companions provides the strongest foundation. A sober sitter experienced with psychedelic states is especially valuable given the unpredictable onset timing.
Aftercare & integration. The extended duration of 1BP-LSD means residual effects — altered perception, emotional sensitivity, difficulty sleeping — may persist for hours after the peak resolves. Plan for a full rest day following the experience.
In the days following, journaling or talking through the experience with a trusted person can help consolidate insights and process difficult material. If distressing thoughts, perceptual changes, or mood disruption persist beyond a week, consult a mental health professional experienced with psychedelic experiences.
Recovery & Support
Classical psychedelics carry low physical dependence risk, but patterns of psychological reliance can develop — using psychedelics to avoid confronting difficult emotions, or compulsive seeking of peak experiences. If psychedelic use is interfering with daily functioning, relationships, or mental health, professional support is warranted.
Resources include the Fireside Project (psychedelic peer support hotline), MAPS integration resources, and psychedelic-informed therapists who can help distinguish productive use from avoidance-driven patterns.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Recognizing an emergency: Most difficult psychedelic experiences are distressing but not medically dangerous. Seek immediate help if: the person is at risk of harming themselves or others, has completely lost contact with reality and cannot be redirected, experiences chest pain or seizures, or expresses intent to act on delusional beliefs.
Immediate steps:
- 1. Stay with the person. Speak calmly and simply.
- 2. Move to a quiet, low-stimulation environment if possible.
- 3. Do not physically restrain unless there is immediate danger of self-harm.
- 4. If symptoms are severe or uncertain, call emergency services.
What to tell the dispatcher: Name the substance (1BP-LSD, an LSD prodrug), the amount taken, the time of ingestion, and current symptoms. Good Samaritan laws in many jurisdictions protect callers from drug-related prosecution.
No reversal agent exists for LSD or its prodrugs. Medical management is supportive: benzodiazepines for severe agitation, a calm environment, and monitoring until effects resolve.
Legal Status[edit]
1BP-LSD occupies a legal grey area in most jurisdictions as of May 2026. LSD is controlled internationally, but the convention does not individually list prodrugs or analogs — national approaches vary widely.
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| Germany | Legal (as of early 2026) | Not covered by the NpSG, BtMG, or AMG. The boron-containing N1 substituent falls outside structural groups defined in the NpSG annex following the 6th amendment (November 2025).[9] May be added via ministerial ordinance at any time. |
| United States | Unscheduled; legally ambiguous | LSD is DEA Schedule I. 1BP-LSD is not explicitly scheduled. The Federal Analogue Act may apply if 1BP-LSD is intended for human consumption and is deemed substantially similar to LSD. As a direct prodrug, this argument is plausible but untested in court. safety citation needed |
| United Kingdom | Likely covered by PSA 2016 | The Psychoactive Substances Act 2016 prohibits producing, supplying, importing, or exporting any substance capable of producing a psychoactive effect. As a prodrug of LSD (Class A under the Misuse of Drugs Act 1971), 1BP-LSD would very likely fall under the PSA. Possession alone is not an offense under the PSA. |
| Canada | Not explicitly listed | LSD is Schedule III of the CDSA. 1BP-LSD is not specifically scheduled. Canada lacks a Federal Analogue Act equivalent. Regulatory status unclear. |
| Australia | Likely prohibited | Australia's broad scheduling approach captures LSD analogs broadly. Based on regulatory treatment of analogous compounds (1P-LSD, 1cP-LSD), 1BP-LSD would likely be captured, though it has not been explicitly listed. |
Analog and prodrug considerations
1BP-LSD converts entirely to LSD in the body,[8] which strengthens the argument for analog classification in jurisdictions with such laws. Legal determination of "substantial similarity" involves considerations beyond pharmacology, however.
In Germany, the compound's legality depends entirely on the specificity of NpSG structural definitions. The failed 2025 attempt to ban all LSD analogs as a group[3] suggests future regulation will continue compound-by-compound — but 1BP-LSD's boron atom may prompt regulators to consider broader structural language.
Legal status changes frequently and without notice. This article is not legal advice.
Safety[edit]
- Acute toxicity
- Low
- Chronic toxicity
- Low
- Withdrawal
- None
- Tolerance buildup
- rapid
- Tolerance reset
- 10 days
- Physical
- None
- Psychological
- Negligible
- Compulsive redosing
- Negligible
- Dose escalation
- Negligible
- Cross-tol.
- LSD · psilo · DMT
No peer-reviewed toxicological, pharmacological, or clinical safety data have been published for 1BP-LSD. All safety information below is inferred from the well-characterized parent compound LSD and the N1-acyl lysergamide prodrug class. The absence of substance-specific data reflects the compound's December 2025 emergence, not a confirmed absence of risk.
Toxicity
Acute toxicity
LSD has no established lethal dose in humans — no confirmed death has been attributed to its direct pharmacological effects despite seven decades of widespread use.[5] Computational toxicity modeling of related N1-acyl LSD analogs predicted oral LD₅₀ values in rats of 49–85 mg/kg — thousands of times above a typical human dose.[25] 1BP-LSD itself was not included in these models. safety citation needed
Breakdown product toxicity
The non-LSD breakdown products of 1BP-LSD hydrolysis include 4-hydroxybenzoic acid (~75 µg per 250 µg dose), a pinacol-type diol (~65 µg), and approximately 6 µg elemental boron as boric acid.[4] All quantities fall far below any known acute toxicity threshold. The long-term effects of repeated boron exposure from chronic use have not been studied.
Psychological risks
Anxiety and panic are the most common acute adverse effects of LSD-class psychedelics, occurring more frequently at higher doses and in unsupported settings.[24] A large survey found that 8.9% of psychedelic users reported functional impairment lasting more than one day, and 2.6% sought medical or psychiatric help.[26]
Acute psychosis can occur in predisposed individuals, particularly those with a personal or family history of psychotic disorders. LSD-precipitated psychosis typically resolves within hours to days but may be prolonged in vulnerable individuals.[7]
Hallucinogen Persisting Perception Disorder (HPPD) is a rare condition in which visual disturbances — geometry, after-images, tracers, visual noise — persist weeks to months after last use.[27][28] Risperidone is specifically contraindicated as it worsens HPPD symptoms.[28]
LSD-class psychedelics can trigger latent psychiatric conditions, particularly schizophrenia-spectrum disorders, in genetically vulnerable individuals.[7]
Tolerance and dependence
Rapid tolerance develops via 5-HT₂A downregulation after a single dose, requiring 7–14 days for full recovery.[6] This rapid tachyphylaxis acts as a biological rate-limiter for frequent use. Cross-tolerance exists across the serotonergic psychedelic class — LSD, psilocybin, mescaline, and other LSD analogs.[12][6]
No physical dependence or withdrawal has been characterized. The rapid tolerance mechanism and the absence of strong dopamine reinforcement make classical psychedelics among the least dependence-forming substance classes.
Drug Interactions
All interaction data is inferred from LSD; no 1BP-LSD-specific interaction studies exist. The extended onset (~2 hours) introduces additional risk: users may take other substances during the delay, assuming 1BP-LSD is inactive.
Lithium co-use is associated with greatly increased difficulty and seizure risk during psychedelic experiences.[26] MAOIs risk enhanced, prolonged, and unpredictable effects through serotonin accumulation. Tramadol carries serotonin syndrome risk.
MDMA increases LSD blood levels (both peak and total exposure), prolongs effects, and produces greater cardiovascular strain — a pharmacokinetic interaction where MDMA inhibits LSD metabolism.[29]
Chronic SSRI/SNRI use reduces psychedelic effects through receptor downregulation, though residual serotonin syndrome risk remains. Antipsychotics block psychedelic effects; risperidone worsens HPPD.[28]
Cannabis produces unpredictable intensification and extension of effects.
Contraindications
8 knownAll contraindications are inferred from LSD and the serotonergic psychedelic class.
Absolute contraindications:
- Personal or family history of psychosis or schizophrenia: LSD-class psychedelics can precipitate acute psychotic episodes and may trigger chronic psychotic illness in predisposed individuals.[7]
- Current lithium use: Associated with significantly increased seizure risk and severe adverse reactions.[26]
- Current MAOI use: Risk of severe, unpredictable serotonergic potentiation.
Relative contraindications:
- Bipolar disorder with psychotic features: Risk of manic or psychotic episode.
- Current mood stabilizer use: Associated with increased risk of challenging experiences.[26]
- Heart conditions: LSD produces moderate increases in heart rate and blood pressure.[24]
- Pregnancy and breastfeeding: No safety data exist. safety citation needed
- Seizure disorders: The interaction between psychedelic-induced brain excitation and lowered seizure thresholds is unstudied. safety citation needed
Harm Reduction[edit]
Forms & Identification
1BP-LSD circulates exclusively as blotter paper. Because blotters are visually identical regardless of their active compound, confirming identity requires reagent testing — and even standard reagent kits may not reliably distinguish 1BP-LSD from other lysergamides on blotter. The boron-containing structure is analytically novel; no published reagent reaction profiles exist for this compound.
The extended onset (2–3 hours) is the most consequential identification challenge in practice: users accustomed to 30–60 minute onsets from LSD or 1P-LSD may interpret the delay as a sign of inactive material and redose prematurely. The result can be a doubled dose arriving as a single wave.
Guidelines
- Test the material using available reagent kits, accepting that results may not distinguish between lysergamides.
- Start with a lower dose — the two-step conversion means individual variation in onset timing and intensity may be greater than with simpler prodrugs.
- Wait at least 3 hours before considering whether effects have fully materialized. Premature redosing is the most common practical risk with slow-onset prodrugs.
- Prepare the environment in advance: comfortable temperature, accessible water, minimal obligations for 14+ hours, no driving requirement.
- Eat a light meal 2–3 hours before dosing. An empty stomach may speed onset; a heavy meal may extend the already long delay unpredictably.
- Tell someone your plan, substance, and dose — even if using alone.
Set & Setting
As with all serotonergic psychedelics, the psychological context (set) and physical environment (setting) are primary modulators of experience quality.[24] The extended come-up of 1BP-LSD places particular demands on both: two hours of uncertainty about whether effects will arrive can generate anticipatory anxiety that colors the entire experience.
A calm, familiar environment with trusted companions provides the strongest foundation. Having a sober sitter — someone experienced with psychedelic states who can offer reassurance without intervention — is especially valuable given the unpredictable onset timing.
Aftercare & integration. The extended duration of 1BP-LSD means residual effects — altered perception, emotional sensitivity, difficulty sleeping — may persist for hours after the peak resolves. Plan for a full rest day following the experience.
In the days following, journaling or talking through the experience with a trusted person can help consolidate insights and process difficult material. If distressing thoughts, perceptual changes, or mood disruption persist beyond a week, consult a mental health professional experienced with psychedelic experiences. Integration circles and psychedelic-informed therapists offer structured support for processing challenging experiences.
Recovery & Support
Classical psychedelics carry low physical dependence risk, but patterns of psychological reliance — using psychedelics to avoid confronting difficult emotions, or compulsive seeking of peak experiences — can develop. If psychedelic use is interfering with daily functioning, relationships, or mental health, professional support is warranted.
Resources include the Fireside Project (psychedelic peer support hotline), MAPS integration resources, and substance-specific harm reduction communities. Mental health professionals trained in psychedelic integration can help distinguish productive use from avoidance-driven patterns.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Recognizing an emergency: Most difficult psychedelic experiences are distressing but not medically dangerous. Seek immediate help if: the person is at risk of harming themselves or others, has completely lost contact with reality and cannot be redirected, experiences chest pain or seizures, or expresses intent to act on delusional beliefs.
Immediate steps:
- 1. Stay with the person. Speak calmly and simply.
- 2. Move to a quiet, low-stimulation environment if possible.
- 3. Do not physically restrain unless there is immediate danger of self-harm.
- 4. If symptoms are severe or you are uncertain, call emergency services.
What to tell the dispatcher: Name the substance (1BP-LSD, an LSD prodrug), the amount taken, the time of ingestion, and current symptoms. Good Samaritan laws in many jurisdictions protect callers from drug-related prosecution.
No reversal agent exists for LSD or its prodrugs. Medical management is supportive: benzodiazepines for severe agitation, a calm environment, and monitoring until effects resolve.
Legal Status[edit]
1BP-LSD occupies a legal grey area in most jurisdictions as of May 2026. LSD is controlled under Schedule I of the 1971 United Nations Convention on Psychotropic Substances, but the convention does not individually list prodrugs or analogs. National approaches vary from compound-by-compound scheduling to broad psychoactive substance bans. The legal status of 1BP-LSD is subject to rapid change without notice.
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| Germany | Legal (as of early 2026) | Not covered by the NpSG, BtMG, or AMG. The boron-containing N1 substituent falls outside structural groups defined in the NpSG annex following the 6th amendment (November 2025).[10] May be added via ministerial ordinance at any time. |
| United States | Unscheduled; legally ambiguous | LSD is DEA Schedule I. 1BP-LSD is not explicitly scheduled. The Federal Analogue Act may apply if 1BP-LSD is intended for human consumption and is deemed substantially similar to LSD. As a direct prodrug, this argument is plausible but untested in court. safety citation needed |
| United Kingdom | Likely covered by PSA 2016 | The Psychoactive Substances Act 2016 prohibits producing, supplying, importing, or exporting any substance capable of producing a psychoactive effect. As a prodrug of LSD (Class A under the Misuse of Drugs Act 1971), 1BP-LSD would very likely fall under the PSA. Possession alone is not an offense under the PSA. |
| Canada | Not explicitly listed | LSD is Schedule III of the CDSA. 1BP-LSD is not specifically scheduled. Canada lacks a Federal Analogue Act equivalent. Regulatory status unclear. |
| Australia | Likely prohibited | Australia's broad scheduling approach captures LSD analogs broadly. Based on regulatory treatment of analogous compounds (1P-LSD, 1cP-LSD), 1BP-LSD would likely be captured, though it has not been explicitly listed. |
Analog and prodrug considerations
1BP-LSD's status as a direct prodrug of LSD — a compound converted to a Schedule I substance in the body — creates distinctive legal questions. The demonstration that N1-acyl LSD prodrugs produce only LSD in human blood[9] strengthens the pharmacological argument for treating these compounds as controlled substance analogs, though legal determination of "substantial similarity" involves considerations beyond pharmacology.
In Germany, the compound's status depends entirely on the specificity of NpSG structural definitions. The failed 2025 attempt to ban all LSD analogs as a group[3] suggests future regulatory action will continue compound-by-compound — but the introduction of a boron atom may prompt regulators to consider broader structural language.
Frequently asked questions
What is 1BP-LSD?
1BP-LSD is a novel lysergamide prodrug of LSD and the first in its class to incorporate a boron atom, active in microgram doses. It undergoes two-step hydrolysis to release LSD, producing a delayed onset of 2–3 hours relative to simpler N1-acyl LSD analogs.
How long does 1BP-LSD last?
Total duration by route of administration — Oral: 10 – 14 hours. Ranges vary with dose and individual factors; see the duration table for onset, peak, and after-effect phases.
Where can I find dosage information for 1BP-LSD?
Psychedex publishes a dosage table for 1BP-LSD on this page covering these routes of administration: oral. Dose values are presented only in that table, always alongside their route of administration.
What are dangerous combinations with 1BP-LSD?
The highest-severity documented interactions for 1BP-LSD: MAOIs (Lethal), Buspirone (Dangerous), Dopamine agonists (Dangerous), GHB, Baclofen (Dangerous), GHB, GBL (Dangerous). See the interactions section for the full list with mechanisms and severity levels.
Is 1BP-LSD addictive?
Psychedex records tolerance and dependence data rather than a yes/no rating. Recorded tolerance indicators for 1BP-LSD: tolerance builds rapid; full reset takes 10 days; cross-tolerance develops with LSD, psilocybin, DMT, mescaline, 1P-LSD, 1B-LSD, 1cP-LSD, 1V-LSD, 1S-LSD. See the article's dependence and safety sections for recorded dependence data.
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First-person accounts of subjective effects, timing, and outcomes — submitted for harm reduction.
references
- [1]
- [2] ^abHolze F, Vizeli P, Müller F, Ley L, Duerig R, Varghese N, Zizzari P, Liechti ME (2021) Acute dose-dependent effects of lysergic acid diethylamide in a double-blind placebo-controlled study in healthy subjects — Neuropsychopharmacology doi:10.1038/s41386-020-00883-6
- [3]
- [4]
- [5]
- [6] ^abcdSchlag AK, Aday J, Salam I, Neill JC, Nutt DJ (2022) Adverse effects of psychedelics: From anecdotes and misinformation to systematic science — Journal of Psychopharmacology doi:10.1177/02698811211069100
references
- [1]
- [2] ^abHolze F, Vizeli P, Müller F, Ley L, Duerig R, Varghese N, Zizzari P, Liechti ME (2021) Acute dose-dependent effects of lysergic acid diethylamide in a double-blind placebo-controlled study in healthy subjects — Neuropsychopharmacology doi:10.1038/s41386-020-00883-6
- [3]
- [4]
- [5]
- [6] ^abcde la Fuente Revenga M, Jaster AM, McGinn J, Silva G, Saha S, Gonzalez-Maeso J (2022) Tolerance and Cross-Tolerance among Psychedelic and Nonpsychedelic 5-HT2A Receptor Agonists in Mice — ACS Chemical Neuroscience doi:10.1021/acschemneuro.2c00170